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certain extent. In his landmark paper on the pathological signatures of cerebrovascular amyloid deposition, Stefanos Pantelakis from the Geneva Brain collection, descripted small arterioles and capillaries within the cerebellar cortex affected by this pathology [2] . Similar findings were also reported in a Japanese autopsy study, which found that 14.3% of cerebellar bleeds were associated with cerebral amyloid angiopathy [3] . On the other hand, ruptured and unruptured microaneurysms (miliary aneurysms) associated with intracerebral haemorrhage and hypertension have also been found in the perforating vessels that irrigate the cerebellum (in addition to the basal ganglia, pons, and deep white matter) [4, 5] . In a recently published issue of Cerebrovascular Diseases , Jacques De Reuck and his colleagues reported new interesting data on microangiopathies in the cerebellum [6] – another elegant investigation in the sequel of the neuropathological/ 7T postmortem MRI studies performed by the group. In 104 postmortem brains of elderly subjects with various neurodegenerative and cerebrovascular pathologies, cortical cerebellar microbleeds and microinfarcts were detected on 7T MRI of horizontal sections of a cerebellar hemisphere. These microvascular lesions showed the same burden in cases with (n = 15) versus without (n = 73) amyloid angiopathy. The prevalence and load of both lesions were higher only in cases with pure and mixed vascular dementia without amyloid angiopathy (n = 8). These findings were consistent with the Little is known about the neuropathology and clinical relevance of small vessel disease in the cerebellum, which have somehow been neglected and understudied. This is partly reflected, for example, when vascular neurologists or stroke physicians encounter patients with spontaneous (i.e. nontraumatic) parenchymal haemorrhage in the cerebellum – determining the predominant underlying microangiopathy contributing to the bleed is not straightforward. In a rather simplistic, but practical way, sporadic small vessel disease in the brain has been traditionally categorised as either cerebral amyloid angiopathy or ‘hypertensive arteriopathy’ [1] . Cerebral amyloid angiopathy is a predominantly superficial pathology affecting cortical and leptomeningeal small vessels due to amyloid-β deposition. Hypertensive arteriopathy, an umbrella term including arteriolosclerosis, lipohyalinosis, and fibrinoid necrosis, more often affects the deep arterial perforators (e.g. lenticulostriate) supplying the basal ganglia, thalami and brainstem structures. Paralleling this distribution, it is commonly considered that strictly lobar macrobleeds or microbleeds are more likely related to cerebral amyloid angiopathy, whereas deep bleeds are associated with hypertensive arteriopathy. When it comes to the bottom of the brain, the cerebellum, a similar working hypothesis is currently missing. Looking back at the original pathological investigations, both cerebral amyloid angiopathy and hypertensive-related damage seem to affect the cerebellum to a Received: March 1, 2015 Accepted: March 17, 2015 Published online: May 7, 2015

Microvascular Lesions at the Bottom of the Brain: New Neuropathological Insights